Category Archives: Disease - Page 22

The Danger of Hospital Food

Posted by on November 8, 2010 10 comments

In the book we discuss how high blood sugar is a powerful predictor of poor outcomes in hospital patients.

Well, Abby’s grandmom is in the hospital with pneumonia. She is being fed with intravenous glucose, and has developed high blood sugar – 160 mg/dl – despite provision of insulin.

Abby says the doctors aren’t concerned. But they should be.

High Blood Sugar Causes Pneumonia

High blood glucose and high insulin both suppress immune function. As a result, pneumonia rates are much higher in hospital patients with high blood sugar. If hyperglycemia helps cause pneumonia, it’s surely a danger in someone who already has pneumonia.

A recent paper investigating the health effects of high blood sugar during total parenteral (meaning intravenous) nutrition gives us a quantitative assessment of the risks of elevated blood sugar. [1]

They report that pneumonia was the number one consequence of elevated blood sugar from intravenous feeding:

In multivariate analysis adjusting for age, sex, and history of diabetes, the blood glucose within 24 h of TPN >180 mg/dl was associated with increased risk of pneumonia (OR 3.6, 95% CI 1.6–8.4) and acute renal failure (2.2, 1.02–4.8 1) compared with patients with blood glucose <120 mg/dl. [1]

In other words: If 24 hours after intravenous feeding is started, blood glucose rises over 180 mg/dl, the likelihood of subsequently contracting pneumonia is increased 3.6 fold.

Abby’s grandma had blood glucose of 160 mg/dl, which is still at elevated risk [1]:

Here the measure is mortality, not pneumonia, but we can see that blood glucose in the range 150-180 mg/dl 24 hours after initiation of TPN is quite a bit more dangerous than blood glucose levels below 150 mg/dl.  Mortality rates are almost 50% higher.

This is not a new finding:

TPN therapy has been associated with increased risk for infections and mortality (2,10–13). The increased risk of complications appears to be related, among other factors, to the development of hyperglycemia (4,14). Observational studies have reported a 33% mortality rate in TPN patients who developed hyperglycemia (15), as well as an increased risk of cardiac complications, infections, systemic sepsis, and acute renal failure (3,4,6). In agreement with these reports, we found a strong correlation between TPN-induced hyperglycemia and poor clinical outcome. [1]

Some of the reasons hyperglycemia is dangerous involve immune suppression:

The mechanisms underlying the detrimental effects of hyperglycemia relate to alterations in immune functions and inflammatory response (16,17). Hyperglycemia impairs leukocyte function, phagocytosis, and chemotaxis (18). Hyperglycemia also increases counterregulatory hormones, inflammatory cytokines, and oxidative stress (16,17), which can lead to endothelial dysfunction and cardiovascular complications (17). [1]

Significance for Treatment

Patients who need intravenous feeding, in pneumonia cases presumably due to high choking risk or need for oxygen, have great difficulty avoiding negative health consequences. But the risks of intravenous feeding are increased by suboptimal formulations that have too much sugar and too much omega-6 polyunsaturated fat. Such formulations can strongly suppress immune function, especially if they produce hyperglycemia.

I hesitate to second-guess doctors who are on the scene and privy to case knowledge, but I think the evidence is pretty strong for the dangers of hyperglycemia. If Abby’s grandma has enough muscle and fat, fasting and receiving parenteral water, vitamins, and minerals might be a better strategy. At a minimum, glucose provision should be reduced or insulin increased to reduce blood glucose levels.

Doctors are Enslaved to Faulty Practice Standards

The paper I cited is from 2010, but the dangers of hyperglycemia have been known for decades. Yet hospitals still commonly induce it.

Our current medical institutions seem to have left doctors terrified of deviating from standard practice, even if standard practice is known to be harmful. And new, better practices can’t be adopted until proven in costly clinical trials, even though the existing practices were adopted without such trials.

I wonder what Dr. House would do in Abby’s grandma’s case? And if Dr. House would do the right thing for the patient in defiance of standard practice, how long would he keep his medical license or his malpractice insurance?

References

[1] Pasquel FJ et al. Hyperglycemia during total parenteral nutrition: an important marker of poor outcome and mortality in hospitalized patients. Diabetes Care. 2010 Apr;33(4):739-41. http://www.ncbi.nlm.nih.gov/pubmed/20040658.

The Vanderbilt Protocol for Multiple Sclerosis

Posted by on November 8, 2010 31 comments

The antibiotic approach to MS therapy was developed at Vanderbilt by Drs. Stratton and Mitchell. They have patented multiple versions of their protocol, most recently in 2005. (Since patents are publicly available and the “Description of the Invention” is often an excellent overview of the science, we’ve put links to patents at the end of this post.)

Since we have some readers with MS, including Alexander, I thought I would post a summary of the Vanderbilt protocol. This was written by Dr. Stratton in 2009:

Treatment Protocol for Chronic Infections Caused by C. pneumoniae

As far as the Cpn Antimicrobial Regimen is concerned, my thoughts (as of 2009) are as follows:

First, as a general rule, the sicker a patient is, the slower they should go. This is why our early protocol started out with only one antibiotic and one dose, and then gradually adding the next dose/antibiotic as the reactions to each dose/antibiotic became apparent. These reactions appear to be caused by destruction of Chlamydia organisms as well as by the death of some of the infected host cells. Even destruction of elementary bodies by reducing agents such as N-acetyl-cysteine (NAC) can cause these reactions as chlamydial major outer membrane protein (MOMP) is released. MOMP is known to interact with Toll-like receptors (TLRs) and can thus induce the production of cytokines. Moreover, chlamydial cell wall contains LPS, which also interacts with TLRs and induces the production of cytokines. The reaction to anti-chlamydial therapy is sometimes referred to as “die-off” as presumable both chlamydial organisms and host cells are dying. These reactions can be delayed by days to weeks and may include “flu-like symptoms”, arthralgias and myalgias, “hangover-like symptoms (“brain-fog”, nausea, malaise), gastroenteritis (including diarrhea), and (rarely) fever. These reactions are akin to the “leprosy reaction” well described with the therapy of leprosy. The use of prednisone (10-20 mg per day) and/or pentoxifylline (Trental, 400 mg bid or tid), as done for the leprosy reaction, may be beneficial.

I think that all patients should start with supplements/vitamins before they start any antibiotics. Baseline lab studies, including CBC and liver function studies, should be done and these parameters followed every 3-4 months, more frequently (i.e., monthly) for sicker patients. As C. pneumoniae can infect white blood cells and liver cells, potential death of these cells should be monitored in sicker patients. Our initial protocol recommended this. I would add NAC to the supplements. We used amoxicillin, which is degraded in the body to penicillamine (a reducing agent) in our regimen as an anti-elementary body agent, but NAC seems to work equally well and may offer additional benefits in boosting the immune system as well as protecting the liver. As far as supplements/vitamins are concerned, I think Professor David Wheldon’s supplement/vitamin suggestions are very complete and should be the benchmark. Once antibiotics are ready to be started, I would start with a macrolide. We have used Azithromycin because it is easy to give and has become somewhat cheaper since it went off patent. Clarithromycin (500 mg twice a day) or Roxithromycin (300 mg once a day) can be used instead of Azithromycin. I would still give just one 250 mg azithromycin tablet and then wait two weeks to see if there is any reaction to it. Then I would give two tablets, one on Monday and one on Wednesday. Once again I would wait two weeks. I’d continue in this way, adding each dose until the patient was taking 250 mg of azithromycin MWF. If the patient has severe reactions (meaning they can’t work – most people are trying to work and take care of a family while they are on this therapy), I’d slow down the process. After the azithromycin, I’d add doxycycline – again doing this very slowly. Once the patient was taking both azithromycin (250 mg MWF) and doxycycline (100 mg twice a day), I’d start the metronidazole pulses – again, doing these slowly and working up to a once a month pulse of 7 days of metronidazole (500 mg twice a day). Once the patient could do the monthly pulse of metronidazole, I’d add rifampin (300 mg twice a day). Once this was tolerated, I would increase the metronidazole pulse to 14 days, doing so slowly. Eventually, the patient should be able to tolerate metronidazole (500 mg twice a day) on a daily basis. Once a patient could do this regimen without any reactions, I would continue it for at least a year and probably three years for MS patients. It might take a year or two (or longer) to get to the point where there is no reaction to the daily metronidazole, depending on the chlamydial load, followed by 1-3 years of therapy. This might be a 5-year program, but should allow the patient to continue to work with minimal disruption. Patients should also be gradually improving during this time. The sicker the patient is, the longer the therapy is going to be. There is no shortcut. Younger patients who have not been sick as long tend to respond more quickly. ?

With MS patients, due to the possible CNS damage that might occur by going slowly, I would move more quickly unless there were major reactions. This means compressing what might have taken a year into several months. 

The reactions patients have are varied – some are severe enough that they stop the antibiotics. That, of course, defeats the purpose of the therapy. It is very tricky and each patient has to learn his own limitations. When we started our protocol, we were thinking of a hotline to answer questions that are now easily and better answered via the internet (http://Cpnhelp.org). Finally, I don’t think this is the only regimen that will work nor do I think it will work better or faster. It is just what I do in 2009 when treating a patient.

I’ve been informed that the late stages of the protocol have been further refined in 2010. Now, once die-off reactions to the metronidazole subside, Dr. Stratton tries rifabutin or rifampin.

I would agree with Dr. Stratton that nutritional supplements should begin 3-4 months before antibiotics, but would add that our diet should be adopted 3-4 months before antibiotics begin. This is necessary to improve immune response and healing capacity; and to avoid unnecessary cell death and die-off toxicity when antibiotics begin. The eleven ways to enhance immunity, discussed in Step Four of the book, should be routinely practiced.

Simply introducing diet and nutrition alone can lead to significant die-off effects. This shows that the adoption of diet and nutritional supplements is therapeutic in its own right.

On a bad diet, antibiotics are dangerous, as they risk gut dysbiosis and introduction of new co-infections.

Like Dr. Stratton, I think being active at http://cpnhelp.org is essential for anyone on this protocol. Many people at cpnhelp.org have used this protocol, often for years, and their experience can be very helpful.

As Dr. Stratton notes, it takes years to cure MS. It is necessary to be patient and to balance speed of killing pathogens against allowing the body time to recover from die-off effects – toxic bacterial proteins and human cell death. Remember, “the dose makes the poison” – doubling the rate of pathogen killing may quadruple the toxicity effects, so the optimum course is not the one with highest rate of pathogen killing. Every patient has to progress at his own pace. Go as fast as you can but no faster.

There are steps that can be taken to reduce die-off toxicity, such as drinking lots of water and eating salt to help urine excretion, and taking “moppers” such as charcoal, bentonite clay, cholestyramine, or chlorella to help assure that toxins released from the liver through the bile are excreted in feces, not re-absorbed.

Conclusion

MS recovery is not impossible; indeed, many have recovered on this protocol. However, it is long and arduous. Optimizing diet will shorten time to recovery, but it will still take years. 

MS is not the only disease that may be caused by C. pneumoniae. Alzheimer’s dementia, atherosclerosis, stroke, rheumatoid arthritis, and rosacea are all associated with C. pneumoniae infections and may be treatable by Dr. Stratton’s protocol.

Links

“Multiple Sclerosis:  A Curable Infectious Disease?”, July 7, 2010, https://perfecthealthdiet.com/?p=157.

“Is Multiple Sclerosis an Autoimmune Disease?”, July 5, 2010, https://perfecthealthdiet.com/?p=151.

“Eleven Steps for Overcoming Alzheimer’s and Other Chronic Infectious Diseases,” July 1, 2010, https://perfecthealthdiet.com/?p=134.

A list of the Vanderbilt patents.

The 2005 patent, ID 7,094,397.

Two From the Web

Posted by on November 4, 2010 21 comments

A few interesting posts elsewhere caught my eye.

First, Dr. Emily Deans reports that people who have experienced influenza or coronavirus infections are much more likely to suffer mood disorders such as depression.

We believe that most diseases result from the interaction of a bad diet with pathogens, so we’re not surprised to see more evidence associating pathogens with depression.

As Dr. Deans says, make sure your vitamin D levels are optimized for protection against these viruses.

Second, Dr. BG offers something tangentially related to our last post on fecal transplant therapies. She links to a post by Richard Nikoley explaining that while in ruminants vitamin B12 is made in the rumen and can be absorbed in the intestine, in carnivores and omnivores like humans vitamin B12 is made in the colon and is not absorbed well, but rather exits in the feces.

This is why animals, in addition to eating a lot of liver if they are carnivores, also eat feces (coprophagia). It gives them vitamin B12. (Perhaps it also cures their colitis, but we’ll await clinical trials to be sure.)

Always eager to provide visual evidence, Dr BG managed to find this video of gorilla coprophagia. Do not watch if you are squeamish, eating dinner, or dislike the sound of children squealing!

More on Fecal Transplants

Posted by on November 3, 2010 43 comments

We’ve had ongoing interest in the topic of fecal transplants from readers of our bowel disease series, and we’ve recently had comments from two biomedical professionals reminding us that it is desirable to have fecal transplants performed by doctors after screening of the stool for pathogens.

Coincidentally, The Scientist ran a nice story today on fecal transplants. [1]

Fecal transplants are effective against C. difficile, ulcerative colitis, and probably other inflammatory bowel disorders:

By producing sturdy spores that can linger in the intestinal tract even after repeated antibiotic treatment, C. difficile can continually give rise to new toxin-producing colonies that wreak havoc on the colon. But these colonies prove no match for fecal transplants, which boast a cure rate of up to 95 percent….

Borody did his first fecal transplant back in the mid 1980s, when he was confronted with one of the most difficult cases he had seen at the time: a woman who had vacationed at Fiji and had developed an incurable colitis through an unknown pathogen.

While searching the literature for alternative treatments, he stumbled upon a paper published in 1958 in the journal Surgery that described four cases in which a similar condition was cured by infusing the inflamed guts of the patients with fecal samples from healthy donors. “So I looked at the method and I kind of made up the rest of it,” Borody said.…

The stool, now turned into slush, was administered to the patient — who had her gastrointestinal tract previously flushed — via two enemas over the course of two days.

The results were nothing short of surprising, Borody said. Within days her colitis was gone, never to return.

It’s a well-proven procedure in animals. Veterinarians don’t bother to screen rumen fluid for pathogens, and yet the procedure is almost always healthful for the recipient:

The procedure, which has deep roots in veterinary science, has been tried and tested in animals for centuries. Farmers handling livestock have long realized, for example, that indigestion following a change in diet in grazing animals, such as cows, can be treated by feeding the sick cow rumen fluid that has been sucked out of a healthy cow’s stomach.

Yet it’s hard to find doctors who will perform the procedure for any ailment except C. difficile infections:

Currently, while most fecal transplants in the U.S. are performed exclusively to treat C. difficile, a growing list of doctors, such as Lawrence Brandt, chief of Gastroenterology at Montefiore Medical Center in New York, are beginning to expand to other gut disorders such as inflammatory bowel diseases….

“It is currently considered a last resort,” he said. But he hopes that will soon change. “It’s relatively simple, relatively inexpensive, and it’s very rapid in its actions.”

Conclusion

In chronic infections of the colon, fecal transplants should be among the first treatments resorted to, not the last resort.

This is one treatment where experience with animals and human patients, demonstrating that fecal transplants are fairly safe and often highly effective in colonic disorders, should trump the normal regulatory barriers to new procedures.

However, given the cautious nature of regulators and most doctors, it seems unlikely that the therapy will be widely available any time soon.

It’s good to hear that there is a “growing list” of doctors who will perform a fecal transplant. Anyone with a seemingly incurable colonic disease should seek one of them out.

References

[1] Cristina Luiggi, “Same Poop, Different Gut,” The Scientist, Nov 3, 2010, http://www.the-scientist.com/news/display/57795/.